ABSTRACT
Intravascular thrombosis is one of the most frequent pathological events affecting mankind and a
major cause of morbidity and mortality in developed countries. There is abundant evidence
suggesting that platelets play a pivotal role in the pathogenesis of arterial thrombotic disorders,
including unstable angina (UA), myocardial infarction (MI), and stroke [1-3]. The underlying
pathophysiological mechanism of these processes has been recognized as the disruption or
erosion of a vulnerable atherosclerotic plaque leading to local platelet adhesion, activation, and
subsequent formation of partially or completely occlusive platelet thrombi. Moreover, large-scale
clinical trials have documented the benefit of antiplatelet therapy in acute coronary syndromes
[1,4,5]. Aspirin is the prototypical platelet inhibitor that blocks thromboxane A2-dependent
platelet aggregation, and represents the standard reference compound for the management of
acute MI, UA, and secondary prevention of MI [1]. Newer-generation antiplatelet drugs, such as
ticlopidine and clopidogrel, which are adenosine diphosphate (ADP) receptor antagonists, have
also been introduced in clinical practice [4]. Although all of the aforementioned agents have
demonstrated clinical benefit, significant mortality still occurs, presumably because they are not
effective against platelet aggregation in response to all agonists. The final common step in
homotypic platelet aggregate formation, regardless of the stimulus, involves the interaction of
the adhesive proteins such as fibrinogen and von Willebrand’s factor (vWF) with the platelet GP
IIb=IIIa receptor [6,7]. Hence, this platelet integrin receptor has emerged as a rational therapeutic target in the management of acute coronary syndromes.
